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@ARTICLE{Tang:182766,
      author       = {W. C. Tang and S. W. Tsao and G. E. Jones and X. Liu and M.
                      H. Tsai and H.-J. Delecluse$^*$ and W. Dai and C. You and J.
                      Zhang and S. C. M. Huang and M. M. Leung and T. Liu and Y.
                      P. Ching and H. Chen and K. W. Lo and X. Li and C. M. Tsang},
      title        = {{L}atent {M}embrane {P}rotein 1 and macrophage-derived
                      {TNF}α synergistically activate and mobilize invadopodia to
                      drive invasion of nasopharyngeal carcinoma.},
      journal      = {The journal of pathology},
      volume       = {259},
      number       = {2},
      issn         = {0022-3417},
      address      = {Bognor Regis [u.a.]},
      publisher    = {Wiley},
      reportid     = {DKFZ-2022-02906},
      pages        = {163-179},
      year         = {2023},
      note         = {2023 Feb;259(2):163-179},
      abstract     = {Invadopodia are actin-rich membrane protrusions that digest
                      the matrix barrier during cancer metastasis. Since the
                      discovery of invadopodia, they were visualized as localized
                      and dot-like structures in different types of cancer cells
                      on top of a 2D matrix. In this investigation of Epstein-Barr
                      virus (EBV)-associated nasopharyngeal carcinoma (NPC), a
                      highly invasive cancer frequently accompanied by neck lymph
                      node and distal organ metastases, we revealed a new form of
                      invadopodium with mobilizing features. Integration of
                      live-cell imaging and molecular assays revealed the
                      interaction of macrophage-released TNFα and EBV-encoded
                      latent membrane protein 1 (LMP1) in co-activating the
                      EGFR/Src/ERK/cortactin and Cdc42/N-WASP signaling axes for
                      mobilizing the invadopodia with lateral movements. This
                      phenomenon endows the invadopodia with massive degradative
                      power, visualized as a shift of focal dot-like digestion
                      patterns on a 2D gelatin to a dendrite-like digestion
                      pattern. Notably, single stimulation of either LMP1 or TNFα
                      could only enhance the number of ordinary dot-like
                      invadopodia, suggesting that the EBV infection sensitizes
                      the NPC cells to form mobilizing invadopodia when
                      encountering a TNFα-rich tumor microenvironment. This study
                      unveils the interplay of EBV and stromal components in
                      driving the invasive potential of NPC via unleashing the
                      propulsion of invadopodia in overcoming matrix hurdles. This
                      article is protected by copyright. All rights reserved.},
      keywords     = {Epstein-Barr virus infection (Other) / invadopodia (Other)
                      / invasion (Other) / latent membrane protein 1 (Other) /
                      live-cell imaging (Other) / nasopharyngeal carcinoma (Other)
                      / tumor-associated macrophage (Other)},
      cin          = {F100},
      ddc          = {610},
      cid          = {I:(DE-He78)F100-20160331},
      pnm          = {316 - Infektionen, Entzündung und Krebs (POF4-316)},
      pid          = {G:(DE-HGF)POF4-316},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:36420735},
      doi          = {10.1002/path.6036},
      url          = {https://inrepo02.dkfz.de/record/182766},
}